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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aortoventriculoplasty is a new method of treatment for left ventricular outflow tract obstructions. The concept is based on creating a surgical defect which is patched in such a way as to provide the largest possible outflow to the left ventricle. The incision of the aorta continues down as far as necessary, with the right ventricular wall, the aortic ring, and the septum being cut. Reconstruction with an inner Dacron patch on the septum is completed by replacing the aortic valve with an adequate prosthesis, covering the aortic incision with the same patch, and patching the right venticular opening with an outer patch. This method was used in 4 children with tunnel-like subaortic stenosis, 3 of whom had had unsuccessful previous surgical attempts. Other associated lesions including parachute mitral valve were also corrected during aortoventriculoplasty. Hemodynamic results were excellent following this operation. Two patients died postoperatively, one from advanced myocardial damage and progressive failure and the other from cerebral ischemia caused by insufficient retrograde perfusion through an aortic coarctation that was not repaired earlier. No arrhythmias were observed following the procedure. The other 2 patients are well 7 and 5 months postoperatively with excellent hemodynamic function.
J Thorac Cardiovasc Surg 1976 Jun
PMID:Aortoventriculoplasty: a new technique for the treatment of left ventricular outflow tract obstruction. 13 85

A case of cerebral ischemia secondary to carotid artery stenosis produced by a subintimal hematoma following blunt trauma to the neck is presented. A carotid endarterectomy with removal of the thrombus and intima was performed with satisfactory recovery of the patient. The various mechanisms involved in producing such stenoses and occlusions are reviewed.
J Cardiovasc Surg (Torino)
PMID:Common carotid artery stenosis due to subintimal hematoma following blunt trauma to the neck. Report of a case. 86 66

Stenosis of the innominate artery usually occurs in older patients in whom the risks of conventional, corrective procedures such as transthoracic endarterectomy or aorto-innominate arterial bypass grafting are quite high. An axillo-axillary bypass procedure was performed in a high-risk patient with innominate arterial stenosis who had repeated episodes of transient cerebral ischemia due to decreased blood flow through the right carotid artery and reversal of blood flow through the right vertebral artery. Postoperatively, he has had dramatic improvement in his symptoms. Because of its simplicity, avoidance of major thoracotomy, avoidance of temporary occlusion of the carotid artery, and excellent late results, axillo-axillary bypass grafting is being proposed as the procedure of choice for stenosis of the innominate artery.
J Thorac Cardiovasc Surg 1975 Feb
PMID:Extrathoracic bypass for stenosis of innominate artery. 108 46

Four patients are reported in whom the aortic arch and variable portions of the ascending and descending aorta were replaced with a prosthesis. In three patients the preoperative diagnosis was dissecting aneurysm of the aortic arch and in one an arteriosclerotic aneurysm of the aortic arch was present. A combination of surface cooling and cardiopulmonary bypass was utilized to produce total body hypothermia. Arch replacement was carried out during a period of total circulatory arrest. Cardiopulmonary bypass was then utilized to warm the patient and resuscitate the heart. The average duration of cerebral ischemia was 43 minutes and the average duration of myocardial ischemia was 74 minutes. The average lowest esophageal temperature was 14 degrees C., and the average lowest rectal temperature was 18 degrees C. Three patients are alive and well 4 to 13 months following surgery. One patient died 4 days postoperatively of pulmonary insufficiency. This experience indicates that by utilizing total body hypothermia and circulatory arrest aortic arch replacement can be carried out with an acceptable mortality rate. Corrective surgery could be offered to patients with life-threatening enlarging aneurysms of the aortic arch.
J Thorac Cardiovasc Surg 1975 Dec
PMID:Prosthetic replacement of the aortic arch. 118 83

Blood pressure and clinical status of 1,736 patients with cerebrovascular disease were observed during 12 months of treatment with nicardipine. The most common diagnoses were chronic cerebral ischemia (53.2%), transient ischemic attacks (TIA; 25.1%), and cerebral infarct (8.7%); 50.1% of patients were classed as hypertensive [systolic blood pressure (SBP) > or = 160 mm Hg or diastolic blood pressure (DBP) > or = 90 mm Hg]. Most patients (91.2%) received a daily dose of 60 mg nicardipine. Additional treatments included diuretics (37%), beta-blockers (11.5%), other antihypertensive drugs (15.8%), platelet antiaggregants (25.1%), and cardiotonic drugs (15.1%). A total of 282 patients (16.2%) were lost to follow-up, 21 (1.2%) patients withdrew due to side effects, 32 (1.8%) died, and 9 (0.5%) patients had treatment interrupted due to concomitant illness. In the hypertensive subgroup, blood pressure (SBP/DBP) was reduced from a mean baseline value of 175 +/- 22/97 +/- 14 mm Hg to 152 +/- 17/85 +/- 11 mm Hg at 3 months and 149 +/- 23/81 +/- 11 mm Hg after 12 months of treatment. The incidence of TIA or stroke among these patients was reduced from 29 cases (3.5%) during the first 3 months to 11 cases (1.54%) during months 4-12 (p < 0.01). In normotensive patients there were 18 (2.15%) cases during months 1-3 and 13 (1.55%) cases during months 4-12 (difference not significant). In the 280 patients treated with nicardipine alone, the most frequent side effects during the first month were facial flushing (6.8%), gastrointestinal problems (5%), dizziness (3.2%), headache (3.2%), drowsiness (3.2%), and hypotension (1.1%). Most of these side effects were transient.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1990
PMID:The influence of nicardipine in patients with high risk of stroke. 136 3

A review is given of the normal regulation of cerebral blood flow (CBF) and its pathophysiology in hypertension and stroke. In otherwise healthy hypertensive patients, the absolute level of CBF is the same as in normal subjects. CBF autoregulation, however, is shifted towards higher pressure, thus impairing the tolerance to hypotension. In most patients, this does not interfere with the beneficial effect of treatment, i.e., stroke prevention. Cerebral ischemia, however, may be provoked by overzealous pressure lowering in selected clinical settings: initial or intensified treatment of very severe hypertension, treatment of hypertension in the elderly, and treatment of hypertension in acute stroke. In the latter, a complicated sequence of brain ischemia and hyperemia makes antihypertensive intervention difficult in the early phase, when blood pressure is probably best allowed to decrease spontaneously.
J Cardiovasc Pharmacol 1992
PMID:Regulation of cerebral blood flow in health and disease. 138 71

Cerebrovascular infarction can be subdivided into two different categories: cerebral hemorrhage and cerebral ischemia. Although the use of calcium antagonists for the treatment of subarachnoid hemorrhage has been established in many series, the benefit of these drugs for the treatment of cerebral hemorrhage is inconclusive, and we lack considerable evidence of its application in acute ischemic stroke. Inconclusive data have been reported from experimental studies using different pharmacological models and different protocols; however, various clinical studies have suggested that calcium antagonists may be useful in improving the neurological and functional outcome of the patient due to reduced infarct size and the properties of the drug to improve tissue metabolism in remote cortical territories. So far, however, these studies failed to establish the efficacy of the drug unequivocally. This may be due to the considerable amount of patients included with small or rapidly recovering neurological deficits and to the delay between onset of symptoms and start of treatment (ranging between 48 and 72 h).
J Cardiovasc Pharmacol 1991
PMID:New aspects of calcium antagonists for treatment of cerebrovascular disease. 172 6

The role of endothelin-1 (ET-1) in cerebral ischemic injury remains the subject of much debate. Vasoconstriction in large conduit vessels may not be associated with reductions in flow at the tissue level. We present two studies examining the effects on local cerebral blood flow of topical application of ET-1 to the surgically exposed middle cerebral artery (MCA) in adult male Sprague-Dawley rats. In the first series using 14C-iodoantipyrine autoradiography, 10 min following application of ET-1 (1 nmol) to the MCA, up to 80% reduction in blood flow in the territory of distribution of the MCA is seen (e.g., dorsolateral caudate nucleus--flow reduced from 131 +/- 3 ml/100 g/min to 29 +/- 25 ml/100 g/min). These levels of flow are comparable with those seen with permanent bipolar diathermy occlusion and division of the proximal MCA--a standard rat model of focal cerebral ischemia. In a second series using hydrogen clearance technique for measurement of local cerebral blood flow in the caudate nucleus, we have shown that flow ipsilateral to application of ET-1 (0.25 nmol) is significantly reduced compared with saline controls for 80 min. Such reduction of flow, at the tissue level, sustained over this duration is consistent with the induction of ischemic cell damage by ET-1.
J Cardiovasc Pharmacol 1991
PMID:Reduction in local cerebral blood flow induced by endothelin-1 applied topically to the middle cerebral artery in the rat. 172 79

The central hemodynamic effects of the peptide endothelin-1 (ET-1) have been investigated in the conscious, normotensive rat. Intracisternal administration of ET-1 (0.01-0.03 nmol) gave rise to an increase in mean arterial pressure with minimal effects on heart rate and was accompanied in some cases by barrel rolling activity. Intracisternal administration of 0.03 nmol ET-1 gave rise to a significant elevation in plasma noradrenaline and adrenaline levels. This elevation in plasma catecholamines was present only in those animals that also exhibited marked behavioral changes. Autoradiographic measurement of cerebral blood flow carried out during the maximum response to 0.03 nmol of intracisternal ET-1 revealed a widespread and profound ischemia throughout the caudal brainstem. Cerebral ischemia is known to activate compensatory circulatory reflexes in the medulla oblongata that result in increased sympathetic and vagal outflow. This is the most likely cause of intracisternal ET-1-induced hypertension. ET-1 is unique in its ability to override the brain's autoregulatory mechanisms and induce ischemia of pathological magnitude.
J Cardiovasc Pharmacol 1991
PMID:Endothelin-1-induced hypertension: a consequence of medullary ischemia? 172 22

The knowledge obtained from the ongoing investigational trials of tPA for acute ischemic stroke will not only help establish the appropriate dose range and complication rates but will also further develop the clearly mandatory rapid, aggressive team approach needed to truly treat acute ischemic strokes successfully. Experimental cerebral ischemia data have pointed to the need to treat acute clinical stroke within only a few hours or less to effectively reduce stroke morbidity and mortality. Specifically, with reversible MCA occlusion models of focal cerebral ischemia (dogs and cats), the animals uniformly survive without neurological deficit if the occlusion is for less than 2 to 3 hours. Similarly in primates, MCA occlusion for 3 hours or less will lead to clinical improvement and a decrease in infarct size, with complete recovery generally associated with less than 2 hours of MCA occlusion. Therefore, it appears unlikely that ischemic brain can be salvaged if vascular occlusion persists longer than 4 to 6 hours (similar to the pathophysiology of myocardial ischemia). Further, at least one third of ischemic stroke patients reperfuse spontaneously (and obviously too late) within 48 hours of stroke onset. Several factors believed to be related to successful outcome after thrombolytic therapy are summarized in Table 16. A schematic approach to determining the response to thrombolytic agents in acute ischemic stroke is outlined in Table 17. Zivin succinctly reviews thrombolysis for stroke, both experimental and clinical, and summarizes some of the difficulties of the early clinical stroke trials with thrombolytic agents and speculates about future prospects. He believes tPA may prove valuable in the treatment of some forms of thromboembolic stroke. Its usefulness may depend in part on how quickly the drug can be initiated and the risk of side effects; factors that will require further study. The currently used doses of tPA may be too low to lyse large cerebral arterial clots and, therefore, if current trials do not show a positive treatment response, further trials with higher doses may be indicated. The implications of a potentially effective treatment for truly acute stroke are enormous: stroke will need to be considered by all (lay public through to caregivers) as a true medical emergency, analogous to MI and trauma.(ABSTRACT TRUNCATED AT 400 WORDS)
Prog Cardiovasc Dis
PMID:Thrombolytic therapy in cerebrovascular disorders. 172 86


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